Persistent Organic Pollutants Exposure Research Articles

Progress in research of relationship between metal or metalloid and persistent organic pollutants exposures and cardiovascular disease

Cardiovascular disease (CVD) is the leading cause of mortality and healthy life expectancy loss, ranking first in causing the global burden of disease. In addition to the traditional CVD risk factors, such as hypertension and diabetes, environmental chemical pollutants may also play a role in the development of CVD. This paper summarizes the evidence regarding the relation of exposures to metal or metalloid and persistent organic pollutants with risk for CVD and introduces the research progress in the relation between the exposures to two environmental chemical pollutants and CVD risk. The study aims to provide scientific evidence for the effective prevention of CVD through the management of chemical pollutants in environment.

A Realistic Mixture of Persistent Organic Pollutants Affects Zebrafish Development, Behavior, and Specifically Eye Formation by Inhibiting the Condensin I Complex.

Persistent organic pollutants (POPs) are posing major environmental and health threats due to their stability, ubiquity, and bioaccumulation. Most of the numerous studies of these compounds deal with single chemicals, although real exposures always consist of mixtures. Thus, using different tests, we screened the effects on zebrafish larvae caused by exposure to an environmentally relevant POP mixture. Our mixture consisted of 29 chemicals as found in the blood of a Scandinavian human population. Larvae exposed to this POP mix at realistic concentrations, or sub-mixtures thereof, presented growth retardation, edemas, retarded swim bladder inflation, hyperactive swimming behavior, and other striking malformations such as microphthalmia. The most deleterious compounds in the mixture belong to the per- and polyfluorinated acids class, although chlorinated and brominated compounds modulated the effects. Analyzing the changes in transcriptome caused by POP exposure, we observed an increase of insulin signaling and identified genes involved in brain and eye development, leading us to propose that the impaired function of the condensin I complex caused the observed eye defect. Our findings contribute to the understanding of POP mixtures, their consequences, and potential threats to human and animal populations, indicating that more mechanistic, monitoring, and long-term studies are imperative.

Exposure to persistent organic pollutants in Danish pregnant women: Hormone levels and fetal growth indices

This study examines possible associations of maternal Persistent Organic Pollutants (POP) exposure during pregnancy, maternal hormone levels and fetal growth indices (FGI). During 1st trimester, we measured maternal thyroids, androgens and estrogens, lipophilic POP and perfluorinated-alkyl-acid (PFAA) levels in serum from nulliparous women. Adjusted multivariate-linear regression models assessed associations between exposure and outcomes. Maternal characteristics and POP exposures associated with maternal hormone levels. Lipophilic POP elicited inverse association with androgen and estrogen levels but no strong association with thyroids. Higher level of PFAA was associated with higher thyroid and androgen levels. The PFAA did not associate with estrogens. Higher thyroid-peroxidase-antibody (TPO-Ab) and estradiol level associated with higher birth weight and length in sons. For daughters, the TPO-Ab associations were the opposite being inversely associated with birth weight and length, and higher TPO-Ab and estradiol associated with lower gestational age. Mediation analyses suggested that TPO-Ab mediates the association of PFAA with FGI.

Prenatal exposure to persistent organic pollutants and changes in infant growth and childhood growth trajectories

BackgroundChildren are born with a burden of persistent organic pollutants (POPs) which may have endocrine disrupting properties and have been postulated to contribute to the rise in childhood obesity. The current evidence is equivocal, which may partly because many studies investigate the effects at one time point during childhood. We assessed associations between prenatal exposure to POPs and growth during infancy and childhood. MethodsWe used data from two Belgian cohorts with cord blood measurements of five organochlorines [(dichlorodiphenyldichloroethylene (p,p’-DDE), hexachlorobenzene (HCB), polychlorinated biphenyls (PCB-138, -150, −180)] (N = 1418) and two perfluoroalkyl substances [perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS)] (N = 346). We assessed infant growth, defined as body mass index (BMI) z-score change between birth and 2 years, and childhood growth, characterized as BMI trajectory from birth to 8 years. To evaluate associations between POP exposures and infant growth, we applied a multi-pollutant approach, using penalized elastic net regression with stability selection, controlling for covariates. To evaluate associations with childhood growth, we used single-pollutant linear mixed models with random effects for child individual, parametrized using a natural cubic spline formulation. ResultsPCB-153 was associated with increased and p,p’-DDE with decreased infant growth, although these results were imprecise. No clear association between any of the exposures and longer-term childhood growth trajectories was observed. We did not find evidence of effect modification by child sex. ConclusionOur results suggest that prenatal exposure to PCB-153 and p,p’-DDE may affect infant growth in the first two years, with no evidence of more persistent effects.

Persistent Organic Pollutant Exposure and Thyroid Function among 12-Year-Old Children

Introduction: Polychlorobiphenyls (PCBs), organochlorine pesticides (OCPs), and per- and polyfluoroalkyl substances (PFASs) are persistent organic pollutants (POPs) having numerous toxicological properties, including thyroid endocrine disruption. Our aim was to assess the impact of POPs on thyroid hormones among 12-year-old children, while taking puberty into consideration. Methods: Exposure to 7 PCBs, 4 OCPs, and 6 PFASs (in µg/L), and free tri-iodothyronine (fT3, pg/mL), free thyroxine (fT4, ng/dL), and thyroid-stimulating hormones (TSH, mIU/L) were assessed through blood-serum measurements at age 12 years in 249 boys and 227 girls of the PELAGIE mother-child cohort (France). Pubertal status was clinically rated using the Tanner stages. For each POP, associations were estimated using linear regression, adjusted for potential confounders. Results: Among boys, hexachlorobenzene and perfluorodecanoic acid were associated with decreased fT3 (log-scale; β [95% confidence interval] = -0.07 [−0.12,−0.02] and β = −0.03 [−0.06,−0.00], respectively). Intermediate levels of perfluorohexanesulfonic acid (PFHxS) and PCB180 were associated, respectively, with increased and decreased fT4. After stratification on pubertal status, PCBs and OCPs were associated with decreased TSH only in the more advanced Tanner stages (3–5) and with decreased fT3 among early Tanner stages (1–2). Among girls, PFHxS was associated with decreased TSH (log-scale; β = −0.15 [−0.29,-0.00]), and perfluorooctanoic acid was associated with decreased fT3 (β_{2nd_tercile} = −0.06 [−0.10,-0.03] and β_{3rd_tercile} = −0.04 [−0.08,-0.00], versus. 1st tercile). Discussion: This cross-sectional study highlights associations between some POPs and thyroid function disruption, which appears consistent with the literature. Considering that the associations were sex-specific and moderated by pubertal status in boys, complex endocrine interactions are likely involved.

Levels of persistent organic pollutants in breast milk samples representing Finnish and Danish boys with and without hypospadias

Hypospadias is a congenital malformation of penile urethra with unknown etiology in most cases. Persistent organic pollutant (POP) exposure may disrupt endocrine function during a critical window of development of male genitalia. In animal studies, POPs have been associated with male reproductive disorders, including hypospadias, but only few studies have assessed this relationship in humans. The aim of this study is to investigate the association between hypospadias and POP concentration levels in breast milk, as a proxy for prenatal exposure. This is a nested case-control study of Danish and Finnish mother-son pairs. Maternal breast milk samples were collected between 1997 and 2002, and they represent infant boys born with hypospadias [n = 33 (n = 22 Danish and n = 11 Finnish)] and their 1:1 matched controls. Breast milk samples were analyzed for six classes of POPs [including dioxins, polychlorinated biphenyls, flame retardants and perfluorinated alkylated substances (PFAS)]. We estimated odds ratios (ORs) and 95% confidence intervals (CI) for each chemical class using conditional logistic regression. In addition, a composite exposure score system was used to explore the effect of a POP mixture (four chemical classes): The composite score was categorized as low, moderate, or high exposure, and differences between cases and controls were tested with conditional logistic regression. No statistically significant associations were observed between the sums of the chemical classes and hypospadias in either country. The composite score was unable to detect differences in the risk of hypospadias between the tertiles of POP exposure. Levels of PFAS were significantly higher in Danish than in Finnish breast milk samples. This small study does not provide evidence for an association between hypospadias and exposure to POPs but adds information on quantitative exposures. Further development of multi-exposure models is needed for assessing the potential mixture effect associated with multiple chemical exposures.

Persistent organic pollutant exposure contributes to Black/White differences in leukocyte telomere length in the National Health and Nutrition Examination Survey

Despite racial disparities in diseases of aging and premature mortality, non-Hispanic Black Americans tend to have longer leukocyte telomere length (LTL), a biomarker of cellular aging, than non-Hispanic White Americans. Previous findings suggest that exposure to certain persistent organic pollutants (POPs) is both racially-patterned and associated with longer LTL. We examine whether Black/White differences in LTL are explained by differences in exposure to 15 POPs by estimating the indirect effect (IE) of self-reported race on LTL that is mediated through nine polychlorinated biphenyls (PCBs), three furans, and three dioxins, as well as their mixtures. Our study population includes 1,251 adults from the 1999–2000 and 2001–2002 cycles of the cross-sectional National Health and Nutrition Examination Survey. We characterized single-pollutant mediation effects by constructing survey-weighted linear regression models. We also implemented various approaches to quantify a global mediation effect of all POPs, including unpenalized linear regression, ridge regression, and examination of three summary exposure scores. We found support for the hypothesis that exposure to PCBs partially mediates Black/White differences in LTL. In single-pollutant models, there were significant IEs of race on LTL through six individual PCBs (118, 138, 153, 170, 180, and 187). Ridge regression (0.013, CI 0.001, 0.023; 26.0% mediated) and models examining summative exposure scores with linear combinations derived from principal components analysis (0.019, CI 0.009, 0.029; 34.8% mediated) and Toxic Equivalency Quotient (TEQ) scores (0.016, CI 0.005, 0.026; 28.8% mediated) showed significant IEs when incorporating survey weights. Exposures to individual POPs and their mixtures, which may arise from residential and occupational segregation, may help explain why Black Americans have longer LTL than their White counterparts, providing an environmental explanation for counterintuitive race differences in cellular aging.

Persistent organic pollutant exposure and associations with gene expression in northern fur seals (Callorhinus ursinus) from St. Paul Island, Alaska

Persistent organic pollutants (POPs) are highly lipophilic compounds that accumulate at increased concentrations in high tropic level organisms like marine mammals. Marine mammals’ reliance on blubber makes them susceptible to accumulating POPs at potentially toxic concentrations. In this study, we analyzed POP concentrations, (polychlorinated biphenyls (PCBs), organochlorine pesticides (OCPs), polybrominated diphenyl ethers (PBDEs), and methoxylated-BDE (MeOBDE), in the blubber of 16 subsistence harvested sub-adult, male northern fur seals as well as assessed changes in mRNA gene expression of nine relevant biomarkers including the aryl hydrocarbon receptor, thyroid receptor-α, and adiponectin. PBDE and MeOBDE concentrations were significantly lower than PCB and OCP concentrations. A negative relationship was observed between percent lipid in the blubber and contaminant concentrations, both individual and sum. Expression changes in eight biomarkers were correlated with individual and sum contaminant concentrations. This study shows that contaminant concentrations measured are correlated to changes in expression of genes from different physiological systems, metabolism and endocrine, that are important for the regulation of blubber metabolism. Northern fur seals are reliant on blubber as an energy source during times of low food intake. Potential contaminant induced changes in blubber metabolism pathways could have significant impacts on the health of individuals during critical periods.

Exposure of zebrafish to an environmental mixture of persistent organic pollutants triggers an increase in anxiety-like syndrome but does not affect boldness in unexposed offspring.

Polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) are persistent organic pollutants (POPs) that are present as complex mixtures in all environmental compartments, including aquatic ecosystems. However, little is known about the effects of such complex mixtures on teleost behaviour. In this study, zebrafish (Danio rerio) were chronically exposed to an environmentally relevant mixture (MIX) containing 22 PCB and 7 PBDE congeners through diet from 5days post fertilization onwards. MIX-exposed F0 fish produced offspring (F1 and F2 generations) that were fed using plain food and grown until adulthood. In each generation, five behavioural traits (i.e. boldness, activity, sociality, exploration and anxiety) were evaluated by the mean of different experimental set-ups. Two distinct behavioural syndromes were identified: boldness, positively correlated to activity and exploration; and anxiety, associated with low sociality. F0 fish did not display any behavioural disruption resulting from POP exposure whereas F1 MIX fish were bolder than fish from other generations but did not differ significantly from F1 controls. F2 MIX fish displayed a higher anxiety syndrome than F2 controls. This is of particular importance since such behavioural changes in offspring generations may have persistent ecological consequences, may affect fitness and hence cause detrimental effects on wild fish populations exposed to POP mixtures.

Exposure to environmental contaminants and folic acid supplementation intergenerationally impact fetal skeleton development through the paternal lineage in a rat model.

Persistent organic pollutants (POPs) are ubiquitous in the environment, which is of concern since they are broadly toxic for wildlife and human health. It is generally accepted that maternal prenatal folic acid supplementation (FA) may beneficially impact offspring development, but it has been recently shown that the father's exposures also influence the health of his offspring. Bone is an endocrine organ essential for whole-body homeostasis and is susceptible to toxicants. Herein, we tested the hypotheses that prenatal paternal exposure to POPs induces developmental bone disorders in fetuses across multiple generations and that FA supplementation attenuates these disorders. We used a four-generation rat model, in which F0 founder females were divided into four treatment groups. F0 females were gavaged with corn oil or an environmentally-relevant POPs mixture and fed either a control diet (2 mg FA/kg), or FA supplemented diet (6 mg FA/kg) before mating and until parturition (four treatments in total). After the birth of the F1 litters, all F0 females and subsequent generations received the FA control diet. Staining with alcian blue and alizarin red S of male and female fetal skeletons was performed at Gestational Day 19.5. Paternal direct and ancestral exposure to POPs delayed bone ossification and decreased the length of long limb bones in fetuses. Maternal FA supplementation did not counteract the POPs-associated delayed fetal ossification and reduced long bone length. In conclusion, prenatal paternal POPs exposure causes developmental bone abnormalities over multiple generations, which were not corrected by maternal FA supplementation.

Persistent organic pollutant exposure and thyroid function among 12-year-old children

Background and aim Polychlorinated biphenyls (PCBs), organochlorine pesticides (OCPs) and per- and polyfluoroalkyl substances (PFASs) are persistent organic pollutants (POPs) globally spread in environment with numerous toxicological properties, including thyroid endocrine disruption. We aimed to assess the associations between various POPs and thyroid hormones among boys and girls aged 12 years, accounting for puberty stages. Methods Exposure to 4 PCBs, 3 OCPs and 6 PFASs was assessed through blood-serum measurements at age 12 in 476 children of the PELAGIE mother-child cohort (France). Thyroid function was assessed in blood-serum by measuring free triiodothyronine (fT3), free thyroxine (fT4) and thyroid-stimulating hormones (TSH). Puberty status was assessed by clinical examination according to the Tanner stages. Associations were estimated with linear regression for each POPs and each hormone (both log-transformed), and adjusted for potential confounders. Exposure levels were categorized when a non-linear dose-response relation was suggested. Analyses were performed for girls (n=227) and boys (n=249) separately. Results Among boys, hexachlorobenzene and Perfluorodecanoic acid were associated with decreased fT3 (β=-0.07 95%CI=[-0.12,-0.02] and β=-0.03 95%CI=[-0.06,-0.00] respectively). Perfluorohexanesulfonic acid (PFHxS) was associated with increased fT4, with higher beta coefficients for the 2nd tercile (compared to 1st tercile reference). After stratification on pubertal Tanner stages, PCBs and OCPs seemed associated with increased TSH in the early puberty group (stages 1 and 2); but, decreased TSH in the stage 3 and late puberty group (stages 4 and 5). Among girls, PFHxS was associated with decreased TSH (β=-0.15 95%CI=[-0.29,-0.00]) and Perfluorooctanoic acid was associated with decreased fT3 (β=-0.06 95%CI=[-0.12,-0.01]). After stratification on pubertal status, no evidence of heterogeneity has been observed. Conclusions Consistently with literature, this study showed associations between some POPs and thyroid hormone levels. Furthermore, some of these associations seemed heterogenous among boys according to pubertal status. Keywords: persistent organic pollutant, thyroid hormones, adolescence

Association of Prenatal Exposure to Persistent Organic Pollutants and Childhood Lipid Levels: The Rhea Birth Cohort (Greece)

BACKGROUND AND AIM: Lipid disorders in childhood are associated with an earlier onset and greater risk of cardiovascular disease in adulthood. Prenatal exposure to persistent organic pollutants (POPs) has been linked to cardiometabolic risk factors in childhood, but there are limited studies evaluating the persistence of these associations into early adolescence. We assessed the impact of in-utero exposure to POPs on lipid profiles during childhood in the RHEA birth cohort in Greece. METHODS: Maternal serum concentrations of several polychlorinated biphenyls (PCBs), dichlorodiphenyldichloroethene (DDE), and hexachlorobenzene (HCB) were measured in first trimester. We measured triglycerides (TG), total cholesterol (TC), HDL- and LDL-cholesterol at 4, 6, and 11 years. Generalized estimating equations and multivariate regression models assessed the associations with repeated and single time-point measures, respectively. We also tested effect modification by sex. RESULTS: We did not find any strong evidence of lipid levels at age-four being associated to prenatal POPs exposure. DDE exposure in the third tertile (>2846 ng/mL) was associated with higher TC (β= 8.01 mg/dL, 95% CI:1.66, 14.36), HDL (β= 3.25 mg/dL, 95% CI: 0.04, 6.46) and LDL (β= 6.29 mg/dL, 95% CI: 0.78, 11.79). HCB in the second tertile (69 – 102.5 ng/mL) was associated with lower TC (β= -7.27mg/dL, 95% CI: -13.36, -1.19) and HDL (β= -3.34 mg/dL, 95% CI: -6.40, -0.27). We observed strong negative associations between all POPs and age-six TG levels. Similarly, HCB and PCB118 were associated with lower TC and LDL levels at 11 years. In GEE models of repeated outcome measures DDE was associated with higher TC and HDL levels. No clear differences by sex were observed. CONCLUSIONS: Our data indicate that in utero exposures to POPs may be associated with changes in child circulating lipids. These findings require further exploration in other settings and larger cohorts. KEYWORDS: prenatal, POPs, lipids, children

Prenatal exposure to POPs mixtures and DNA methylation alterations in multiple tissues at birth

Background/Aim: Prenatal exposure to persistent organic pollutants (POPs) has been linked to adverse health conditions in the offspring. However, little is known about the underlying mechanisms. Growing literature suggests epigenetics may play a role. We aimed to evaluate the associations of prenatal exposure to individual POPs exposure and POP mixtures with global and site-specific DNA methylation (DNAm) changes in cord blood and placenta in the Early Autism Risk Longitudinal Investigation (EARLI) study. Methods: We leveraged existing data on maternal serum POPs collected during early pregnancy and cord blood (n=122) and placenta DNAm (n=80) measured on the Illumina 450K platform at birth. Concentrations of 11 polychlorinated biphenyls (PCBs), 4 polybrominated diphenyls (PBDEs), and 2 persistent pesticides were measured. We examined global DNAm in 5 genomic regions (genome wide, open sea, shelf, shore, and island regions) and site-specific DNAm at 261 loci previously identified to be associated with POPs. Linear regression and quantile g-computation models were performed to evaluate the single pollutant effect and joint effect of POP mixtures on DNAm adjusted for surrogate variables and confounders. Results: Prenatal exposure to PCB 28 was associated with decreased placental DNAm levels at sites located in shelf regions (p=0.04). There was an inverse linear relationship observed between POP mixtures and placental DNAm in open sea regions. POP mixtures were associated with a decrease in methylation levels at 5 sites in cord blood and 14 sites in placenta and an increase in methylation levels at 4 sites in cord blood at nominal level. None of these associations was significant after FDR adjustment. Conclusions. We observed global DNAm changes in placenta associated with prenatal exposure to PCB 28 and POP mixtures. The findings suggest DNAm involvement in response to prenatal environmental exposures in developmentally relevant tissues. Keywords: Persistent organic pollutants, chemical mixtures, DNA methylation, quantile g-computation

Persistent organic pollutant exposure contributes to Black/White differences in leukocyte telomere length: Evidence from NHANES 1999-2002

Persistent organic pollutant exposure contributes to Black/White differences in leukocyte telomere length: Evidence from NHANES 1999-2002

Exposure to several polychlorinated biphenyls (PCBs) is associated with chronic kidney disease among general adults: Korean National Environmental Health Survey (KoNEHS) 2015-2017.

We investigated the association between major persistent organic pollutants (POPs) exposure and chronic kidney disease (CKD) among general adult population of Korea. For this purpose, a subset of the adult population (n=1276) participated in Korean National Environmental Health Survey (KoNEHS) Cycle 3 (2015-2017) were analyzed for twenty-four POPs in serum, including organochlorine pesticides (OCPs), polychlorinated biphenyls (PCBs), and polybrominated diphenyl ethers (PBDEs), and were derived for estimated glomerular filtration rate (eGFR) and urinary albumin-to-creatinine ratio (uACR). Multivariable linear regression was conducted to assess the association between POPs exposure and CKD-related parameters including eGFR and uACR. As sensitivity analyses, principal component analysis was conducted. Moreover, the U.S. National Health and Nutrition Examination Survey (NHANES) 1999-2004 data were chosen to compare with the observations of the Korean adults. Approximately 7.7% of the Korean adult population possessed CKD based on either eGFR (<60ml/min/1.73m2) or uACR (≥30mg/g) criteria. Among the POPs that were detected in ≥70% of the subjects, PCB153 (β=-1.61, 95% CI: -2.55, -0.67, P=0.001) and PCB180 (β=-1.47, 95% CI: -2.53, -0.40, P=0.007) exhibited significant associations with decreased eGFR, especially in females. In male participants, hexachlorobenzene (HCB) was associated with eGFR (β=-0.79, 95% CI: -1.53, -0.04, P=0.040). Sex-dependent associations with eGFR were also shown in the PCA model. Moreover, the sex-dependent associations of PCBs were similarly observed in the adult populations of the US NHANES. However, POPs exposure was not associated with uACR, regardless of association model or population. The observed associations of PCBs are supported by several experimental studies reported elsewhere. To our knowledge, it is the first report that suggests significant associations of PCBs and HCB with eGFR among general population, and further validations in other populations are warranted.

Exposure to a human relevant mixture of persistent organic pollutants or to perfluorooctane sulfonic acid alone dysregulates the developing cerebellum of chicken embryo.

Prenatal exposure to persistent organic pollutants (POPs) is associated with neurodevelopmental disorders. In the present study, we explored whether a human-relevant POP mixture affects the development of chicken embryo cerebellum. We used a defined mixture of 29 POPs, with chemical composition and concentrations based on blood levels in the Scandinavian population. We also evaluated exposure to a prominent compound in the mixture, perfluorooctane sulfonic acid (PFOS), alone. Embryos (n=7-9 per exposure group) were exposed by injection directly into the allantois at embryonic day 13 (E13). Cerebella were isolated at E17 and subjected to morphological, RNA-seq and shot-gun proteomics analyses. There was a reduction in thickness of the molecular layer of cerebellar cortex in both exposure scenarios. Exposure to the POP mixture significantly affected expression of 65 of 13,800 transcripts, and 43 of 2,568 proteins, when compared to solvent control. PFOS alone affected expression of 80 of 13,859 transcripts, and 69 of 2,555 proteins. Twenty-five genes and 15 proteins were common for both exposure groups. These findings point to alterations in molecular events linked to retinoidXreceptor (RXR) signalling, neuronal cell proliferation and migration, cellular stress responses including unfolded protein response, lipid metabolism, and myelination. Exposure to the POP mixture increased methionine oxidation, whereas PFOS decreased oxidation. Several of the altered genes and proteins are involved in a wide variety of neurological disorders. We conclude that POP exposure can interfere with fundamental aspects of neurodevelopment, altering molecular pathways that are associated with adverse neurocognitive and behavioural outcomes.

Organohalogenated Substances and Polycyclic Aromatic Hydrocarbons in Fish from Mediterranean Sea and North Italian Lakes: Related Risk for the Italian Consumers.

The primary source of persistent organic pollutant (POP) exposure is food, especially fish. European seabass (Dicentrarchus labrax) and gilthead seabream (Sparus aurata) are among the most eaten sea fish in Italy. Fish from lakes in Northern Italy, such as agone (Alosa agone), represent niche consumption for most people, but possibly constitute a much larger percentage of overall consumption volume for local residents. This study dealt with the presence of POPs in the above-mentioned fish species via GC-MS/MS analysis. None of the analytes for which maximum limits are in place showed concentrations above those limits. Moreover, none of the substances without maximum limits exceeded the provisional tolerable daily intake (PTDI) when given, nor did they exceed the more general values considered safe, even for 99th percentile consumers.

Serum concentrations of persistent organic pollutants mixture during pregnancy and anogenital distance in 8-year-old children from the INMA-Asturias cohort

BackgroundDuring pregnancy, women are commonly exposed to several endocrine-disrupting chemicals, including persistent organic pollutants (POPs). These compounds can transfer to the fetus through the placenta. Prenatal POP exposure is related to altered fetal genital and reproductive tract development. However, the relationship between exposure to POP mixtures and anogenital distance (AGD) is poorly investigated. This study investigated the association between prenatal exposure to POP mixtures and AGD in 8-year-old children. MethodsData were collected from the INMA-Asturias cohort. Maternal serum POP concentrations were measured during the first trimester of pregnancy. Anoscrotal distance (AGDAS) and anopenile distance (AGDAP) in males and anofourchetal distance (AGDAF) and anoclitoral distance (AGDAC) in females were recorded in 362 8-years-olds. Conventional linear regression, and the novel weighted quantile sum regression (WQSR) and Bayesian kernel machine regression (BKMR) models were applied to assess the relationships between AGD and POPs exposure stratified by sex. ResultsAmong males, in the linear regression, b-hexachlorocyclohexane, PCB138, PCB153, and PCB180 were inversely associated with the anogenital index (AGI)AS (−0.06 mm/kg (95% confidence interval [CI]: –0.11, −0.02), −0.07 mm/kg (95% CI: –0.14, −0.01), −0.07 mm/kg (95% CI: –0.13, −0.01), and −0.08 mm/kg (95% CI: –0.14, −0.02), respectively). Among females, polybrominated diphenyl ether (PBDE)47 and PBDE154 were positively associated with increased AGIAF (0.02 mm/kg (95% CI: 0.00, 0.03) and 0.09 mm/kg (95% CI: 0.01, 0.17), respectively). BKMR confirmed these associations. WQSR found a negative combined effect of the POP mixture on AGD, and PCB138, PCB153, and PCB180 (weighted 0.18, 0.13, and 0.09, respectively) were identified as the most impacting chemicals. In females, WQSR found a positive combined effect and determined PBDE47 (weighted 0.35) as the most impacting. ConclusionsMaternal exposure to a POP mixture was negatively associated with AGD in male children and positively associated with AGD in female children, thus providing evidence of the adverse effects of POPs on genital development.

Sexually Dimorphic Accumulation of Persistent Organic Pollutants in Fetuses.

Living in an industrialized era, we are exposed to man-made chemicals including persistent organic pollutants (POPs). Previous studies have shown associations of POP exposure with adverse outcomes in humans, wildlife, and the environment, making it a global concern. Exposure during sensitive windows of susceptibility such as fetal development is of particular concern because of the potential increased risk of developing diseases in childhood and adulthood. However, there are limited studies on the sexual dimorphism of POP accumulation during the prenatal period. In this mini-review, we focus on differences in POP concentrations in the placenta and fetal tissues between males and females. We also show the sexually dimorphic adverse outcomes of prenatal exposure to POPs. Overall, our summary shows that males may accumulate higher concentrations of POPs in the placenta and fetal tissues compared to females, although studies are sparse and inconsistent. In addition, there are differences in adverse health outcomes associated to prenatal POP exposure according to sex. Hence, we highly urge researchers investigating the health effects of POP exposure to consider sexual dimorphism in their studies.

Is Glacial Meltwater a Secondary Source of Legacy Contaminants to Arctic Coastal Food Webs?

Climate change-driven increases in air and sea temperatures are rapidly thawing the Arctic cryosphere with potential for remobilization and accumulation of legacy persistent organic pollutants (POPs) in adjacent coastal food webs. Here, we present concentrations of selected POPs in zooplankton (spatially and seasonally), as well as zoobenthos and sculpin (spatially) from Isfjorden, Svalbard. Herbivorous zooplankton contaminant concentrations were highest in May [e.g., ∑polychlorinated biphenyls (8PCB); 4.43, 95% CI: 2.72–6.3 ng/g lipid weight], coinciding with the final stages of the spring phytoplankton bloom, and lowest in August (∑8PCB; 1.6, 95% CI: 1.29–1.92 ng/g lipid weight) when zooplankton lipid content was highest, and the fjord was heavily impacted by sediment-laden terrestrial inputs. Slightly increasing concentrations of α-hexachlorocyclohexane (α-HCH) in zooplankton from June (1.18, 95% CI: 1.06–1.29 ng/g lipid weight) to August (1.57, 95% CI: 1.44–1.71 ng/g lipid weight), alongside a higher percentage of α-HCH enantiomeric fractions closer to racemic ranges, indicate that glacial meltwater is a secondary source of α-HCH to fjord zooplankton in late summer. Except for α-HCH, terrestrial inputs were generally associated with reduced POP concentrations in zooplankton, suggesting that increased glacial melt is not likely to significantly increase exposure of legacy POPs in coastal fauna.